CCNB1 and cancer: Our data showed a dose-dependent decrease in p-Akt (and t-Akt) and its upstream activator PI3K (catalytic subunit) and an increase in Fas (death receptor), suggesting that the FBA-TPQ stimulus -suppresses the PI3K-Akt (p-Akt) pathway and phosphorylates MDM2 to regulate the expression of growth factors (E2F1, Rb, p21 and p27, etc.)or apoptotic (PARP, Bcl-2, Bax and caspase-3, etc.)and cell cycle related (CDC25C,CDK1 and Cyclin B1, etc.)proteins, resulting in the compound's sustained anti-cancer effects.